Dysarthria as an isolated neurological manifestation of Vitamin B12 deficiency: An unusual presentation

Sukhaswarup Kanojiya; Mrugal Doshi; C Kaumudi; Arti Muley; Sunil Kumar

doi:10.4103/JIHS.JIHS_25_18

CASE REPORT

Year : 2018 | Volume : 6 | Issue : 2 | Page : 74-76

Dysarthria as an isolated neurological manifestation of Vitamin B12 deficiency: An unusual presentation

Sukhaswarup Kanojiya, Mrugal Doshi, C Kaumudi, Arti Muley, Sunil Kumar
Department of Medicine, S.B.K.S, MIRC, Vadodara, Gujarat, India

Date of Web Publication

26-Feb-2019

Correspondence Address:
Mrugal Doshi
E 401 Asopalav Club Apartments, Behind Vincenza Highbreeze, Kalali, Vadodara - 390 012, Gujarat
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JIHS.JIHS_25_18

Abstract

Vitamin B12 (Vit. B12) is an important cofactor for the cellular metabolism and myelination. Vit. B12 deficiency can manifest as hematological, neurological, or gastrointestinal (GI) abnormalities. The following case had a unique manifestation of Vit. B12 deficiency in the form of dysarthria without any evidence of hematological involvement. From this case, we can infer that, in young patients with isolated neurological manifestation, Vit. B12 deficiency can always be a differential diagnosis. A 26-year-old female presented with complaints of fever, odynophagia, and dysarthria. She was vitally stable and had no neurological deficits. Her blood investigations showed leukopenia and thrombocytopenia. She was positive for dengue immunoglobulin M, her Vit. B12 levels were low, and her hemoglobin electrophoresis was suggestive of sickle-cell trait. She was subjected to an upper GI endoscopy which was suggestive of antral gastritis. Her magnetic resonance imaging findings were within normal limits. Upon intravenous supplementation of Vit. B12, her dysarthria resolved. From the clinical course and investigation, we consider that dysarthria is an isolated neurological manifestation of Vit. B12 deficiency.

Keywords: Dysarthria, odynophagia, Vitamin B12 deficiency

How to cite this article:
Kanojiya S, Doshi M, Kaumudi C, Muley A, Kumar S. Dysarthria as an isolated neurological manifestation of Vitamin B12 deficiency: An unusual presentation. J Integr Health Sci 2018;6:74-6

How to cite this URL:
Kanojiya S, Doshi M, Kaumudi C, Muley A, Kumar S. Dysarthria as an isolated neurological manifestation of Vitamin B12 deficiency: An unusual presentation. J Integr Health Sci [serial online] 2018 [cited 2023 Mar 28];6:74-6. Available from: https://www.jihs.in/text.asp?2018/6/2/74/252877

Background

Vitamin B12 (Vit. B12) is a water-soluble vitamin essential for the synthesis of DNA and cell division.^[1] It has an important role in cellular metabolism as well as in regulating and maintaining the integrity of the nervous system.^[2] Its deficiency results in impaired erythropoiesis and demyelination in the nervous system, which account for most of its clinical manifestations.^[3],[4] Early diagnosis of Vit. B12 deficiency is pivotal for timely management and in preventing long-term complications which could account for significant morbidity. Clinically, Vit. B12 deficiency presents mainly with a spectrum of neurological and psychiatric manifestations.^[5] We report a case of Vit. B12 deficiency in a young patient who presented with dysarthria only.

Case Report

A 26-year-old young female presented to the medicine outpatient department with complaints of fever, painful swallowing, and generalized weakness for 6 days; difficulty in speaking for 4 days; vomiting 6 days back; and loose stools 3 days back. Fever was low grade, intermittent, and not associated with chills or rigors. It used to get relieved by medication. The patient had three to four episodes of nonprojectile vomiting on the 1^st day of illness which was watery in consistency but neither bilious nor blood stained and persisted for 1 day. The patient had three to four episodes of watery diarrhea, but there was no history of blood in stool or exposure or contact. She also had difficulty in speech in the form of dysarthria for 3 days; however, there was no other neurological deficit present at that time.

There was no history of cough, cold, headache, burning micturition, or rashes. There was no history of loss of consciousness, seizure, bowel/bladder involvement, or head trauma. She had no significant past history. Her family history was negative for any hereditary or metabolic disorders. There was no previous history of dysarthria or any other neurological deficit.

On examination, the patient was conscious and oriented. She was afebrile. Pulse rate was 86/minute, regular, and normal in volume and force, and blood pressure was 122/84 mmHg in the right arm in supine position. No pallor, icterus, edema, clubbing, cyanosis, and lymphadenopathy was detected, and no abnormality was detected on systemic examination. There was no neck stiffness, and pupils were normal in size and equally reactive to light.

Her blood investigation on admission revealed mild anemia, leukocytopenia, and thrombocytopenia. Urine routine microscopy was within normal limits. Serum electrolytes had normal values. Renal function tests revealed no abnormality, but liver enzymes were elevated despite normal bilirubin levels. Peripheral smear for malarial parasite was negative [Table 1]. She reported positive for dengue immunoglobulin M. Ultrasonography of the abdomen was normal. Upper gastrointestinal (GI) endoscopy revealed multiple patches of mucosal congestion suggestive of antral gastritis. Rest of the endoscopy was unremarkable. Test with Helicobacter pylori kit was positive. She was given treatment for H. pylori and other supportive treatment. Her symptoms resolved with the treatment, but dysarthria persisted.

Table 1: Laboratory reports of the patient

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Hence, Vit. B12 level was measured which was 94 pg/ml. Sickling test was done as this area receives many patients from nearby areas endemic for sickle hemoglobinopathy. Sickling test was positive. Hemoglobin electrophoresis was suggestive of sickle-cell trait. Magnetic resonance imaging brain with contrast was normal. As no obvious neurological cause of dysarthria could be identified and the patient's Vit. B12 levels were low, intravenous Vit. B12 supplementation was started. Dysarthria showed progressive improvement with it and almost completely recovered after 5 days of the start of Vit. B12 supplementation.

The patient had a total stay of 8 days in the hospital. Her complaints of fever, vomiting, and diarrhea were relieved. Her blood counts including platelet counts came to normal. Her speech showed steady improvement over the due course of her hospital stay. She was discharged after 8 days in a stable condition with normal speech.

Discussion and Conclusion

Vit. B12 deficiency presents with hematological, GI, and neuropsychiatric manifestations. The hematological manifestations include increased mean cellular volume (MCV), ovalo-macrocytosis, and hypersegmented neutrophils.^[6] It has also been observed that only some of the Vit. B12-deficient patients present with the classical abnormality of hematocrit, MCV, and serum lactate dehydrogenase. Moreover, the hallmarks of Vit. B12 deficiency, namely macro-ovalocytes and hypersegmented neutrophils, frequently remain undetected as the latter is mostly seen only in frank Vit. B12 deficiency. They may, however, have no symptoms or have symptoms due to severe anemia such as dyspnea on exertion, easy fatigue, dizziness, and orthostatic hypotension, or those related to congestive heart failure such as pedal edema and orthopnea. Other associated symptoms reported include glossitis leading to painful food intake; altered bowel motility, such as mild diarrhea or constipation; and loss of bladder or bowel control.^[7]

It has been believed that hematological impairment due to Vit. B12 deficiency starts early and precedes neuropsychiatric manifestations.^[8] However, an increasing number of patients have been reported to have neuropsychiatric presentations without any abnormality in hemogram.^[9] The exact mechanism which determines the clinical phenotype (neuropsychiatry or hematological) is not known. Some have suggested that the reason may be the different biochemical properties of methylcobalamin and adenosylcobalamin, the two active forms of Vit. B12. Methylcobalamin and folate undergo reactions responsible for DNA synthesis in cells where chromosomal replication and division occur as in hematological systems.^[10] Whereas, adenosylcobalamin acts as a coenzyme for methylmalonyl coenzyme A mutase needed for the synthesis of fatty acids in the myelin sheaths. This does not require folate that surrounds nerve cells.^[11]

Neuropsychiatric symptoms due to Vit. B12 deficiency are known to occur via multiple pathways 1. Vasculotoxicity and reduction in monoamine production due to reduced synthesis of tetrahydrobiopterin.^[12] 2. Lesions in myelin sheath due to secondary increase in homocysteine and methylmalonic acid concentration.^[13] The main neuropsychiatric manifestations of Vit. B12 deficiency are paresthesia, ataxia, limb weakness, delusions, irritability, and decreased interest. Other manifestations include depression and sleep disturbances.^{[14],[15],[16],[17]} These neurological features are also seen in other illnesses such as HIV, diabetes, syphilis, and alcoholism along with some medications, thus posing a diagnostic challenge.^[18] There have been reports of speech disturbances observed with other neurological manifestations; however, to our knowledge, there is no report of isolated speech disturbance due to Vit. B12 deficiency. This case of Vit. B12 deficiency had two interesting points; it presented with neurological manifestation without hematological involvement and the neurological manifestation also was only dysarthria. The patient responded promptly with the supplementation of Vit. B12 with full recovery within few days. This case emphasizes the importance of increased index of suspicion of Vit. B12 deficiency in young patients presenting with isolated neuropathic symptoms as if detected early and treated adequately in time, the patients have fast and full recovery.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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